Amineral has to be normally occurring, inorganic, solid, have a crystalstructure, and also have a definite chemical composition. Charcoal is no amineral due to the fact that it is carbon-based and came from fossilized plants. Thatproves the it is organic and has no definite chemical composition,defying 2 rules friend would have to follow to it is in a mineral. Glass is anon-crystalline solid. This way that the atoms are not i ordered it in aregular and repeating pattern. A mineral by meaning possess acrystalline form, it has actually its aspects arranged in a consistent andrepeating pattern.

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I found the full exercise top top the internet and also attached is table v the results. The task is: "Identify the defect in each mutant."For mutant 1, the defect is a deletion the the repressor gene. The wt cell contains all the gene that are vital to check the questions for the lac permease protein (that"s why that is supplied in the experiment). V the wt cells the table shows that there to be only, and always, lac permease production as soon as lactose was present. The fact that, when considering the mut1 cell or the wt cells v the mut1 lac operon plasmid (F" lac native wt/mut1), over there was always lac permease manufacturing regardless of the visibility or lack of lactose, and also in the F" lac indigenous mut1/wt cells there wasn"t, tells united state that there is a deletion that the repressor gene operator in the mut1 cells. The repressor binds come the operator as soon as lactose is absent. This is a gene that is outside the operon and also therefore over there is no repression when considering mut1 cells.For mutant 2, the defect is a deletion that the operator. Over there is always production of lac permease protein, even when over there isn"t lactose, which method that over there isn"t an operator because that the repressor to tie to. The operator is component of the operon lac and therefore, if the is not current in mut2"s operon lac, over there won"t ever be repression the this operon.For mutant 3, the defect is a defective promotor. Since there appears to it is in no trouble with the regulation that the operon lac when lactose is absent, and there isn"t any kind of production that lac permease even when lactose is present, the problem is the activation the the operon through the promotor. Once the promotor wt is existing there is no problem and the lac permease production occurs normally.For mutant 4, the defect is a defective CAP-binding site. Once there is a defective CAP-binding site, the lid protein cannot tie to the operon. The cap protein binds to the lac operon anytime glucose is short so that the lac operon is activated.

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As soon as considering only mut4 cell this activation is not present which shows a trouble with this activation process. If over there is normal production of lac permease anytime wt lac operon is present, it means that the problem is ~ above the really binding site of the mut4 operon and not in the lid protein.